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Biomedical subjects

T Nouchi

Publications and source records attributed to T Nouchi.

31 records · Page 2Linked to original sources
PubMed1991

Inhibition of acetaminophen activation by ethanol and acetaldehyde in liver microsomes.

Mechanisms of the inhibitory effect of ethanol on acetaminophen hepatotoxicity are controversial. We studied the effects of ethanol and acetaldehyde, an oxidative metabolite of ethanol, on NADPH-dependent acetaminophen-glutathione conjugate production in liver microsomes. Ethanol at concentrations as low as 2mM prevented the conjugate production noncompetitively. Acetaldehyde also inhibited acetaminophen-glutathione conjugate production at concentrations as low as 0.1mM that is comparable with those observed in vivo after social drinking. Acetaldehyde may be involved in ethanol-induced inhibition of acetaminophen hepatotoxicity.

Acetaldehyde↗
PubMed1991

Appearance of alpha-smooth-muscle-actin-positive cells in hepatic fibrosis.

The appearance of alpha-smooth-muscle-actin (alpha-smA)-positive cells during hepatic fibrosis was studied immunohistochemically in rat and human livers. In the normal rat liver, alpha-smA was observed only in vascular smooth muscle cells. With the progression of fibrosis induced by CCl4 injection, alpha-smA-positive cells appeared in the perisinusoidal space and the fibrous septa, and ultimately surrounded regenerative nodules. An increase of desmin-positive cells was recognized in the fibrotic areas and the perisinusoidal area. In the human liver, alpha-smA-positive cells appeared in the fibrotic area, whereas no desmin-positive cells were observed, except in vascular walls of the central vein and the portal tract, alpha-smA is a good marker for the detection of myofibroblast-like cells, and the appearance of alpha-smA in liver mesenchymal cells seems closely related to the process of hepatic fibrosis in both rat and man.

Actins↗
PubMed1990

Comparison of effectiveness of 3 dithiocarbamates on excretion and distribution of cadmium in rats and mice.

Sodium N-benzyl-D-glucamine dithiocarbamate (BGD), sodium N-p-methylbenzyl-D-glucamine dithiocarbamate (MBGD), and sodium N-p-isopropylbenzyl-D-glucamine dithiocarbamate (PBGD), which were recently synthesized, were evaluated for their efficacy in the distribution and excretion of cadmium in rats and mice exposed to cadmium. Rats and mice were injected i.p. with 109CdCl2 (1 mg Cd/kg and 2 microCi 109Cd/one animal) and 3 days later, they were treated with the dithiocarbamates (400 mumol/kg) every other day for 2 weeks. These dithiocarbamates were effective in removing cadmium from the body without increasing the cadmium content in the kidney. After treatment with BGD, MBGD, and PBGD, cadmium was excreted mainly in the feces and the effect of MBGD and PBGD on the fecal excretion of cadmium was much larger than that of BGD. The treatment with these dithiocarbamates did not cause the redistribution of cadmium to brain, testes, and heart in rats and mice. The treatment of mice with PBGD decreased the concentrations of essential metals in liver, kidney, and brain. The extent of acute toxicity of the dithiocarbamates in mice was in the order PBGD greater than MBGD greater than BGD.

Animals↗
PubMed1990

Novel route to preparation of high purity lysoplasmenylethanolamine.

A rapid and simple method has been developed for the preparation of highly purified lysoplasmenylethanolamine. The starting material, a phosphatidylethanolamine (PE) sample that contained a mixture of the 1, 2 diacyl- and 1-O-alkenyl-2-acyl forms was subjected to mild alkaline methanolysis for 20 min at room temperature. Addition of chloroform and water with vigorous mixing, but without acidification at this point, led to a preferential retention of the lysoplasmenylethanolamine in the alkaline aqueous phase and complete separation of the methyl esters into the chloroform phase. Neutralization of the alkaline phase with dilute acetic acid, followed by addition of chloroform, allowed recovery of the lysoplasmenylethanolamine in the chloroform phase in very high yields (75-80% based on vinyl ether content of starting material). On the other hand, a preparation of cholineglycerophospholipids enriched in plasmenylcholine, treated in exactly the same manner, gave a lysoplasmenylcholine that was not retained in the alkaline phase, but partitioned primarily into the chloroform-rich phase together with the methyl esters. Characterization of the purified lysoplasmenylethanolamine was achieved by thin-layer chromatography and compositional analysis. In addition, fast atom bombardment mass spectral analysis of the intact lysoplasmenylethanolamine together with gas chromatography-mass spectrometry of the dimethyl acetals derived from the 1-O-alkenyl chains allowed further proof of the structure and an assessment of the purity of this compound.

Chromatography, Thin Layer↗
PubMed1988

Desmin distinguishes cultured fat-storing cells from myofibroblasts, smooth muscle cells and fibroblasts in the rat.

To differentiate cultured rat liver myofibroblasts, fat-storing cells, aortic smooth muscle cells and skin fibroblasts from each other, desmin and vimentin stainings were undertaken by indirect immunofluorescence using monoclonal antibodies. In myofibroblasts, the reaction with antibodies to vimentin was positive but that with antibodies to desmin was virtually negative. In primary cultures as well as subsequent passage of fat-storing cells, reactions with antibodies to both desmin and vimentin were positive. In primary culture of smooth muscle cells, both reactions were positive, but in the first passage, smooth muscle cells lost the reactivity with antibodies to desmin. Fibroblasts showed a positive reaction with antibodies to vimentin and a negative one with antibodies to desmin. Thus, immunohistochemistry of intermediate filaments allows for the differentiation between fat-storing cells, which are desmin- and vimentin-positive, and myofibroblasts or fibroblasts, which are desmin-negative but vimentin-positive. Smooth muscle cells are also vimentin-positive and become desmin-negative after the first passage.

Adipose Tissue↗
PubMed1987

Serum procollagen type III N-terminal peptides and laminin P1 peptide in alcoholic liver disease.

The appearance of perivenular fibrosis on liver biopsy reflects the beginning of the fibrotic process that ultimately results in liver cirrhosis. To examine whether the fibrogenic activity can be detected by blood tests, we evaluated whole antibody radioimmunoassay (RIA) of procollagen type III N-terminal peptides (P-III-P), RIA of these peptides using Fab fragments (Fab-P-III-P), and RIA of the laminin P1 peptide in alcoholics within 1 week of alcohol abstinence. The Fab-P-III-P levels in subjects with perivenular fibrosis were significantly higher than those in patients with simple fatty liver. Values in 63% of subjects with perivenular fibrosis exceeded the upper limit of the fatty liver group. Patients with simple fatty liver had significantly lower values than nonalcoholic controls. Serum levels of P-III-P and laminin were elevated in patients with alcoholic hepatitis and correlated well with the degree of inflammation. With abstinence, Fab-P-III-P levels increased in all alcoholics. P-III-P values increased in patients with normal P-III-P values on admission. By contrast, the values of laminin decreased during abstinence. Therefore, to interpret serum levels of Fab-P-III-P, P-III-P, and laminin, the duration of abstinence must be taken into consideration. P-III-P, Fab-P-III-P and laminin measurements in the serum within 1 week of abstinence can contribute to the detection of alcoholic liver disease and the determination of its stage.

Adult↗
PubMed1986

Liver fibrosis in alcoholics. Detection by Fab radioimmunoassay of serum procollagen III peptides.

Radioimmunoassays were used to measure serum levels of laminin and of procollagen III peptides, both with the intact antibody and with the Fab fragments, within one week of alcohol withdrawal in 83 alcoholics admitted for detoxification and/or treatment of concomitant medical problems. All patients underwent a diagnostic liver biopsy, which revealed simple fatty liver in 22, perivenular fibrosis in 20, septal fibrosis in 21, and cirrhosis in 20. Although all three serum measurements correlated significantly with the degree of fibrosis, only the Fab radioimmunoassay of procollagen III peptides discriminated between simple fatty liver and perivenular fibrosis in a significant number of subjects.

Adult↗
PubMed1985

Increased hepatotoxicity of acetaminophen by concomitant administration of caffeine in the rat.

Since caffeine is frequently co-administered with acetaminophen, it is of clinical interest to study the effect of caffeine on the hepatotoxicity of acetaminophen. In male Sprague-Dawley rats fasted for 18 h, concomitant administration of caffeine (0.1 g/kg, i.p.) as judged by increased serum enzyme activities and increased incidence of hepatic necrosis. Careful observations on hepatotoxicity are suggested when acetaminophen is prescribed with caffeine.

Acetaminophen↗
PubMed1984

Fatal intoxication by 1,2-dichloroethane--a case report.

This is a case report of acute fatal intoxication after accidental exposure to 1,2-dichloroethane in a 51-year-old man. Clinical manifestations, blood chemistry, and autopsy findings are described. High levels of lactate and ammonia in blood had been observed before the elevation of glutamic transaminases, lactic dehydrogenase, and creatine phosphokinase. Ornithine carbamyl transferase and glutamic oxaloacetic transaminase of mitochondrial origin (m-GOT) were remarkably high.

Accidents, Occupational↗
PubMedDate not supplied

Activation of acetaminophen oxidation in rat liver microsomes by caffeine.

Addition of caffeine in vitro stimulated the oxidative metabolism of acetaminophen by rat liver microsomes, resulting in increased formation of acetaminophen-glutathione (GSH) conjugates and increased covalent binding of acetaminophen to microsomal protein. This metabolic enhancement by caffeine was most prominent using liver microsomes from phenobarbital (PB)-treated rats. Liver microsomes obtained from rats treated with ethanol-oxidized acetaminophen at much faster rates than microsomes from control, PB-treated or 3-methylcholanthrene (3-MC)-treated animals. The stimulatory effect of caffeine was, however, minimal in liver microsomes obtained from ethanol-treated rats.

Acetaminophen↗